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Although individualised therapy can treat the signs and symptoms of RA and slow disease progression, there is currently no cure

Current treatment strategies

Current RA Treatment Strategies and Therapies

  • No current treatment cures RA.
    • The goals for RA therapy are therefore remission, a return of full function and the maintenance of remission.1,2
  • The early recognition and treatment of RA is important for minimising disability and maximising quality of life.
    • A delay in treatment of just a few months can result in significantly more joint damage subsequently in the course of disease.3–5
  • Optimal control of RA is best achieved by regular assessments of disease progression every 2−4 months and modifying treatment when necessary.6

Rheumatoid arthritis treatment algorithm

There is a significant unmet clinical need for a treatment that is well tolerated and provides rapid relief and ultimately remission

  • Current therapies for RA fall into two broad categories.7−9
    • Symptomatic treatments (relief from pain and inflammation, but unable to prevent progressive joint damage), for example:
      • Non-steroidal anti-inflammatory drugs
      • Selective cyclooxygenase-2 inhibitors
      • Glucocorticoid drugs, such as prednisolone; these drugs can relieve inflammation and in high doses can have a dramatic effect on the symptoms of RA, but are generally used only temporarily and at low doses because of their association with serious adverse effects.7−8
  • Disease-modifying agents have a demonstrated ability to halt the destructive course of RA and prevent joint damage; this category of drugs can be further subdivided into two groups.
    • Synthetic (non-biologic/traditional/conventional) DMARDs;1,7 these drugs act as general anti-inflammatory and antiproliferative agents by inhibiting folic acid metabolism and increasing extracellular adenosine levels, respectively.6Examples include MTX, leflunomide, sulphasalazine and hydroxychloroquine. These agents are frequently used in dual and triple combination rather than as monotherapy.1
    • Biological agents (biologics); these drugs are immune modulators that directly target the intracellular signalling pathways, cytokines and other mediators contributing to the pathogenesis of RA. Examples include anti-TNFs (adalimumab, etanercept, infliximab, golimumab, certolizumab), B-cell targeted therapy (rituximab), the T-cell co-stimulation modifier abatacept, and tocilizumab, the first biologic therapy to specifically inhibit the IL-6 receptor.
  • Although biologics have revolutionised RA management over the last decade, approximately 30–40% of patients fail to respond or have an inadequate response to current RA therapies.10
  • In addition, many patients are unable to tolerate currently available treatment options.
  • There is thus a significant unmet clinical need for a treatment that is well tolerated and provides rapid relief, and ultimately remission, for a large section of the RA patient population.

References:

  1. O’Dell JR. Therapeutic strategies for rheumatoid arthritis. N Engl J Med 2004; 350:2591–2602.
  2. Smolen J, et al. Treating rheumatoid arthritis to target: recommendations of an international task force. Ann Rheum Dis 2010; 69 (4):631–637.
  3. Lard LR, et al. Early versus delayed treatment in patients with recent-onset rheumatoid arthritis: comparison of two cohorts who received different treatment strategies. Am J Med 2001; 111:446–451.
  4. Egsmose C, et al. Patients with rheumatoid arthritis benefit from early 2nd line therapy: 5 year followup of a prospective double blind placebo controlled study. J Rheumatol 1995; 22:2208–2213.
  5. Tsakonas E, et al. Consequences of delayed therapy with second-line agents in rheumatoid arthritis: a 3 year followup on the hydroxychloroquine in early rheumatoid arthritis (HERA) study. J Rheumatol 2000; 27:623–629.
  6. Smolen JS, et al. Therapeutic strategies in early rheumatoid arthritis. Best Pract Res Clin Rheumatol 2005; 19:163–177.
  7. Gaffo A, et al. Treatment of rheumatoid arthritis. Am J Health Syst Pharm 2006; 63:2451–2465.
  8. Gotzsche PC, Johansen HK. Short-term low-dose corticosteroids vs. placebo and nonsteroidal anti-inflammatory drugs in rheumatoid arthritis. Cochrane Database Syst Rev 2003; CD000189. Accessed February 2009; www.cochrane.org/reviews/en/ab000189.html
  9. Saag KG, et al. Low dose long-term corticosteroid therapy in rheumatoid arthritis: an analysis of serious adverse events. Am J Med 1994; 96:115–123.
  10. Voll RE, Kalden JR. Do we need new treatment that goes beyond tumor necrosis factor blockers for rheumatoid arthritis? Ann N Y Acad Sci 2005; 1051:799–810.

Figure adapted with permission from Elsevier (C) 2005.